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002 - 6201 - Host Defenses > (20) Antiviral Immunity > Flashcards

(20) Antiviral Immunity Flashcards

1
Q

Are both innate and adaptive immunity important for blocking infection and eliminating virally infected cells?

A

yes

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2
Q
  1. What type of cytokines are released in innate immunity to fight viruses?
  2. What cells kill the infected cells in innate immunity? directly or indirectly?
  3. What can b cells do to fight viruses?
  4. What about T cells?
A
  1. type 1 interferon
  2. NK cells; either (indirect uses antibodies)
  3. Release antibodies that neutralize the virus
  4. Tc cells recognize viral epitopes and kill the infected cell
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3
Q

(Anti-Viral Immune Processes)

  1. Adaptive immunity is mediated by what? which do what?
  2. Antibodies allow what
A
  1. mediated by antibodies which block virus binding and entry into host cells
  2. ADCC by NK cells, and by Tc which eliminate infected cells
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4
Q

(Anti-Viral Immune Processes)

  1. Innate immunity does what three things?
  2. What are five means by which it fights viruses?
A
  1. inhibits virus processes, kills infected cells, and activates leukocytes
  2. complement, interferons, NK cells, Cytokines and chemokines, defensins
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5
Q

What do Tc cells secrete to block viral replication?

A

IFN-y

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6
Q

1-4. What do Tc cells release to kill virally infected cells?

  1. Is lysis of virus-infected cells always the answer?
A
  1. perforin - pore
  2. granzymes - serine proteases
  3. granulysin - induce apoptosis
  4. lymphotoxin (LT-a) - apoptosis
  5. NO!
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7
Q
  1. What is one way the viruses interfere with immune responses?
A
  1. by blocking MHC type 1 expression
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8
Q
  1. What do viruses interfere with to promote viral replication?
  2. What are some anti-apoptosis actions?
  3. Why would virus want to keep a cell alive?
A
  1. apoptosis
  2. block MHC 1 presentation, inactivate granzymes, prevent capase activation, production of virokines tha inhibit Tc function
  3. needs to use it to replicate
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9
Q

(Ab-dependent cellular cytotoxicity) (ADCC)

  1. Once a virus is intracellular - is it directly accessible to antibodies?
  2. but many viruses will insert their proteins into the cell membrane as they prepare to bud out of the cell
  3. what does this allow Ab to do? then what happens?

4. What is the main anti-viral activity of NK cells?

A
  1. no
  2. -
  3. Ab can attach to infected host cells; NK cells and macrophages bind and kill the cell

4. secretion of cytokines IFN-a/b and THF-a that activate other cells (not cell lysis!)

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10
Q

Are there viral mechanisms for evading NK cells?

Do we need to know them?

A

yes

it really doesn’t seem that way

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11
Q

1-3. What are the three things that antibodies do the fight viruses (humoral anti-viral immunity)?

  1. So how to B cells get activated?
A
  1. neturalization
  2. opsonization
  3. complement activation
  4. debris is picked up b dendritic cells (for example) - then go to draining lymph nodes and present to B cells
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12
Q
  1. opsonization can be used for what two things?
A
  1. phagocytosis or activation of NK cells
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13
Q

(Ab and Viral Immunity)

viruses evade by antigenic shift

  1. evasion also occurs by the shedding of what from the viral capside protein?
  2. or inclusion of viral proteins in the capside thatn blcock what?
  3. other viral proteins may disrupt the complement cascade
A
  1. shedding of antigen
  2. complement-mediated lysis
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14
Q
  1. Pro-inflammatory property of complement assists with what?
  2. Cleavage products from complement proteins act on blood vessels to increase what?
  3. This is especially important for viral clearance in that what?
  4. In addition virus infected cells can by lysed by what if what?
  5. What else assists in virus-infected cells uptake and degradation by phagocytes?
A
  1. viral clearance
  2. vascular permeability

3. IgG, IgM, and Tc cells can extravasate to sites of inflammation

  1. by complement if antibodies are bound to the cell surface
  2. opsonization of virus-infected cells or particles
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15
Q
  1. Do viruses have ways of inhibiting complement?
  2. what messes with binding of antibody to C1?
  3. what messes with c3/c5 convertase

*they mess up a lot of complement stuff

* he wants us to remember that complement deals with more than anti-bacterial (anti-viral too!)

A
  1. yes
  2. influenza
  3. herpes
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16
Q

(Cytokines and Viral Immunity)

  1. Are cytokines the most important in anti-viral immunity?
  2. What are the most important anti-viral cytokines?
  3. What are another important type?
  4. What does it do?
A
  1. yes
  2. interferons (type 1)
  3. TNF-a
  4. activates and recruits leukocytes

look at slide a little - I have no idea to what depth I need to understand this material!

17
Q

learn this graph

  1. Many viruses can interfere with cytokine signals or use their own version of cytokines to disrupt immunity
  2. Viruses make their own versions cyokines - or do what other two things?
A
  1. make cytokine binding proteins, or induce cellular production of anti-inflammatory cytokines
18
Q

(Anit-viral actions of Interferons)

  1. What do interferons upregulate to aid in virus clearance?
A
  1. MHC class 1 expression
19
Q
  1. Interferons induce expression of several whats?
  2. These are sometimes referred to as what?
  3. What is one of the important enzymes that is turned on? What does this activate? what does this do? How do eurkaryotic cells avoid this?
  4. What is another enzyme that gets activated? what does it do? involved in what? what is the result of phosphorylation? why doesn’t this target the host?
A
  1. anti-viral enzymes
  2. “intrinsic” immune processes of “biochemical” immunity
  3. 2’5’ - OAS (oligo A synthetase); RNase L; degrades mRNA; stops viral gene expression; 5’ cap
  4. PKR (protein kinase R); phosphorylates eIF-2; translation of mRNA into proteins; shuts down protein synthesis; it actually does a little (see decreased protein synth in virally infected cells)
20
Q

(Mx Proteins)

  1. What induces the production of these? Why called this?
  2. Have what activity? generally speaking?
  3. do number of genes vary among species? where does mx1 go? mx2? why needed in both places?
A
  1. type I interferons; derived from myxovirus resistance in mice
  2. GTPase activity; interfere with viral protein production by essentially blocking viral biochemistry
  3. yes; cytoplasm; nucleus; viruses replicate in both of these places
21
Q

(Anti-viral actions of Interferons)

  1. What does 25 OAS do?
  2. what does PKR do?
  3. what do andenosine deaminases (ADAR1) do?
A
  1. RNA degradation
  2. mRNA translation inhibition
  3. edit RNA (take amine groups off of amino acids)
22
Q
  1. OAS25 (oligoadenylate synthetase) activity against viruses is to cause what?
A
  1. digestion of dsRNA
23
Q

Protein Kinase R (PKR) activation by viral dsRNA leads to what?

A
  • phophorylation of transcription elongation factor 2alpha - then shuts off protein synthesis
24
Q

MxA block what?

A

viral replication, perhaps by binding to viral proteins

25
Q

APOBECs (aka ADARs)

  1. what do these mess up?
  2. APOBECs target what type of viruses?
  3. ADARs target what?
  4. main action is to what?
A
  1. the codin sequence for the virus
  2. target DNA’s (either viruses that have DNA in genome or go through cDNA step in replication)
  3. RNA themselves
  4. remove the amine group from cytosine (c to g transition or t to a)
26
Q

(RNA editing)

  1. what is the net effect?
A
  1. introduction of codon changes in viral genome and mRNAs
27
Q

(APOBEC anti-viral infection)

  1. What binds to the APOBEC in the infected cell? so what happens without Vif?
A
  1. Vif; APOBEC can fuck shit up
28
Q
  1. IFN and inflammatory gene expression is induced quickly following viral infection of most cels. Part of this response is due to recognition of what?
  2. What are intracellular pamp receptors? dow what?
A
  1. PAMPS (pathogen-associated molecular patterns) - notably dsRNA for viruses
  2. TLR-3 and a NOD (nucleotide oligomerizaion domain); trigger IFN-a/b transcription
29
Q
  1. Cytoplasmic PAMPs identify what?
  2. RIG-1 binds to the RNAs, which cause it to associate with adapter proteins (MAVS), eventually leading to interferon gene induction through what and other cytokines through what?
A
  1. viral RNAs
  2. IRF-3; NF-kB
30
Q
  1. Nucleic acid sensors within the infected cell active what?
  2. INcludes what kinds of things?
  3. Signal for what?
A
  1. the anti-viral immune response
  2. toll-lie recepotrs and RIG-1 proteins
  3. cytokine production (pro-inflammatory)
31
Q

What is the main cytokine in antiviral immunity?

A

interferon!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

32
Q

(Immunity to Parasites)

  1. immunity to parasites consists of what two things?
  2. What kinds of infections to parasites set up?
  3. Variation in life cycle - which does what?
  4. Innate immunity to parasites include what two things?
A

1, antibodies and mast cells

  1. chronic infections
  2. increases pathogenicity
  3. phagocytosis and reactive or toxic products
33
Q

(Immunity to Parasites)

1-2. Adaptive immunity includes what two things?

  1. Parasites tend to evoke what type of Th1/Th2 responses?
  2. Helminths tend to trigger production of what cytokines? that do what?
A
  1. antibody formation that can opsonize and trigger complement
  2. IgE antibody which binds to mast cells and eosinophils via the Fc regions - these cells will release proteases and vasodilators - particularly important for helminths
  3. very polarized
  4. IL-4 an IL-5 (activates mast cells and eosinophils)
34
Q

(Anti-parasite immunity)

  1. When bound by antibody (esp IgE), eosinophils can attack parasites via their whats? then what occurs?
A
  1. FcyRI; release of toxic granules
35
Q
  1. What type of Th reaction do you want to parasites? why?
A
  1. Th2 - less inflammaotry (less host tissue damage) - favor production o f antibodies (IgE —> mast cells and eosinophils)
36
Q
  1. Cryptosporidium oocysts attach themselves to what?
  2. they use part of the cell membrane to hide themselves
  3. what cell type is important in killing these? why?
A
  1. wallls of animal intestine
  2. gamma/delta T cells (esp in cattle) ; they express stress signals

002 - 6201 - Host Defenses (29 decks)

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